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はじめに
脱髄の機構は多様であり代謝性,中毒性,感染性,アレルギー性など種々の場合が考えられる。ここでは中枢神経系のアレルギー性脱髄,すなわち実験的アレルギー性脳脊髄炎Experimental allergic encephalomyelitis(EAE)について最近の知見を中心に論ずる。
EAEには急性型acute formと慢性再発型chronic relapsing formがあり,ヒトの急性散在性脳脊髄炎acute disseminated encephalomyelitis(ADEM)や多発性硬化症multiple selerosis(MS)の動物モデルとして注目されている。まず急性EAEの発症機序について述べる。
Abstract
1. Acute EAE
Acute EAE has been induced by immunizing animals with BP/CFA. The fundamental pathogenesis is known to be delayed type hypersensitivity to BP, and the disease can be transferred to a recipient with sensitized cells. The transfer is enhanced by in vitro activation with BP. The technique was applied to study the mechanism of tolerance. Since acute EAE can be transferred to a naive recipient with reactivated lymph node cells obtained from animals recovered from acute EAE, the tolerance cannot be explained by clonal deletion.
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